C h a p t e r 1 4
Mechanisms of Infectious Disease
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listeriosis, and Legionnaires’ disease, are adapted to
survive and reproduce within phagocytic white blood
cells after ingestion, avoiding or neutralizing the usu-
ally lethal products contained within the lysosomes of
the cell.
H. pylori
, the infectious cause of gastritis and
gastric ulcers, produces a urease enzyme on its outer cell
wall. The urease converts gastric urea into ammonia,
thus neutralizing the acidic environment of the stom-
ach and allowing the organism to survive in this hostile
environment.
Other unique strategies used by pathogenic microbes
to evade immunologic surveillance have evolved solely
to avoid recognition by host antibodies. Strains of
S. aureus
produce a surface protein (protein A) that
immobilizes immunoglobulin G (IgG), holding the anti-
gen-binding region harmlessly away from the organ-
isms. This pathogen also secretes a unique enzyme
called
coagulase.
Coagulase converts soluble human
coagulation factors into a solid clot, which envelops and
protects the organism from phagocytic host cells and
antibodies.
H. influenzae
and
N. gonorrhoeae
secrete
enzymes that cleave and inactivate secretory IgA, neu-
tralizing the primary defense of the respiratory and
genital tracts at the site of infection.
Borrelia
species,
including the agents of Lyme disease and relapsing fever,
alter surface antigens during the disease course to avoid
immunologic detection.
Invasion Factors
Infectious agents also produce invasive factors that
facilitate the penetration of anatomic barriers and host
tissue. Most invasive factors are enzymes capable of
destroying cell membranes (e.g., phospholipases), con-
nective tissue (e.g., elastases, collagenases), intercellular
matrices (e.g., hyaluronidase), and structural protein
complexes (e.g., proteases). The effects of the pathogen’s
invasive factors and toxins, combined with the antimi-
crobial and inflammatory substances released by host
cells, mediate the tissue damage and pathophysiology of
infectious diseases.
Clinical Presentation
The term
symptomatology
refers to the collection of
signs and symptoms expressed by the host during the
disease course. This is also known as the
clinical pre-
sentation
and can be characteristic of any given infec-
tious agent. In terms of pathophysiology, symptoms
are the outward expression of the struggle between
invading organisms and the retaliatory inflammatory
and immune responses of the host. The symptoms of
an infectious disease may be specific and reflect the
site of infection (e.g., diarrhea, rash, convulsions,
hemorrhage, and pneumonia). Conversely, symptoms
such as fever, myalgia, headache, and lethargy are
relatively nonspecific and can be shared by a num-
ber of etiologic agents. The symptoms of a diseased
host can be obvious, as in the case of chickenpox or
measles. Other, covert symptoms, such as an increased
white blood cell count, may require laboratory testing
to detect. Accurate recognition and documentation
of symptomatology can aid in the diagnosis of an
infectious disease.
Site of Infection
Inflammation of an anatomic location is usually des-
ignated by adding the suffix -
itis
to the name of the
involved tissue (e.g., bronchitis, inflammation of the
bronchi and bronchioles; encephalitis, brain inflam-
mation; carditis, inflammation of the heart). These
are general terms, however, and they apply equally to
inflammation from infectious and noninfectious causes.
The suffix -
emia
is used to designate the presence of a
substance in the blood (e.g.,
bacteremia, viremia
, and
fungemia
describe the presence of these infectious agents
in the bloodstream). The term
sepsis
, or
septicemia
,
refers to the presence of a proven bloodstream infection
combined with a systemic immune response.
The site of an infectious disease is ultimately deter-
mined by the type of pathogen, the portal of entry, and
the competence of the host’s immunologic defense sys-
tem. Many pathogenic microorganisms are restricted
in their capacity to invade the human body.
M. pneu-
moniae
, influenza viruses, and respiratory syncytial
virus rarely cause disease outside the respiratory tract;
infections caused by
N. gonorrhoeae
are generally con-
fined to the genitourinary tract; and
Clostridium dif-
ficile
, shigellosis, and giardiasis seldom extend beyond
the gastrointestinal tract. These are considered local-
ized infectious diseases. The bacterium
Helicobacter
pylori
is an extreme example of a site-specific pathogen.
H. pylori
is a significant cause of gastric ulcers but has
not been implicated in disease processes elsewhere in the
human body. Bacteria such as
N. meningitidis
, a promi-
nent pathogen of children and young adults;
Salmonella
typhi
, the cause of typhoid fever, and
B. burgdorferi
,
the agent of Lyme disease, tend to disseminate from the
primary site of infection to involve other locations and
organ systems. These are examples of systemic patho-
gens disseminated throughout the body by the circula-
tory system.
An
abscess
is a localized pocket of infection composed
of devitalized tissue, microorganisms, and the host’s
phagocytic white blood cells: in essence, a stalemate in
the infectious process. In this case, the dissemination
of the pathogen has been contained by the host, but
white cell function within the toxic environment of the
abscess is hampered, and the elimination of microorgan-
isms is inhibited. Abscesses usually must be surgically
drained to affect a complete cure. Similarly, infections
of biomedical implants such as catheters, artificial heart
valves, and prosthetic bone implants are seldom cured
by the host’s immune response and antimicrobial ther-
apy. The infecting organism colonizes the surface of the
implant, producing a dense matrix of cells, host pro-
teins, and capsular material—a biofilm—necessitating
the removal of the device.
